While obesity has been thought of as a chronic disease by some, until recently, it was not officially recognized as such. Obesity impairs body function, with potentially negative impacts on physical activity and psychological well-being. It lines internal organs with fat, putting stress on the body; fat tissue may cause dysfunctional cell-signaling, potentially increasing inflammation in the body (Front Endocrinol (Lausanne). 2013 Jun 12;4:71).

The American Medical Association has taken an important step forward, declaring obesity a disease, unto itself. Obesity’s prevalence in the U.S. has increased by more than two-fold in the last two decades (JAMA 2010, 303(3):235-24). More than one-third of Americans are obese, defined as a body mass index of great than 30 kg/m2, according to the CDC.

The AMA’s move is a wake-up call that should be taken very seriously. They recognize that the first step to reversing this trend is increasing awareness among the medical community of its independent detrimental effects. This decision may impact government policy, medical reimbursement rates, and the social stigma patients have to withstand.

Unfortunately, obesity is also associated with many other chronic diseases. Integrative medicine physician Mark Hyman, M.D. entitled his book “Diabesity” to emphasize the association between diabetes and obesity. Other diseases associated with obesity include rheumatoid arthritis, cardiovascular disease, nonalcoholic fatty liver disease, osteoarthritis, and infection. I will discuss the RA association in more detail, since obesity was shown to potentially affect RA treatment.

Obesity treatment options include surgery, medications and lifestyle modifications. While it’s important for obese patients to lose weight, we have to be conscious about the way we do this. The drug Fen-phen, for instance, caused pulmonary hypertension and valvular heart disease. Surgery can potentially result in side effects, such as dumping syndrome and malabsorption. Even lifestyle modifications, including exercise and diet, need to be evaluated.

New launching of weight-loss drug

There are now two drugs approved by the FDA for weight-loss: Qsymia (phentermine hydrochloride/topiramate) and Belviq (lorcaserin). Both drugs have extensive side effects. Belviq was just recently launched in the United States (Medscape.com); however, it has not been approved by the European Union for fear of side effects, including tumors, disease of the heart valves and depression. It was also rejected by the FDA the first time because of its side-effect profile.

Effect on rheumatoid arthritis

On June 27 I wrote an article about RA, so I thought it appropriate to write about how RA is intertwined with obesity. A recent study found that greater than 50 percent of women who have RA are also obese (Arthritis Care Res (Hoboken). 2013;65(1):71-7). This was a cohort (those with disease compared to those without) study, involving over 1,400 participants. The reasons for this association may be underlying inflammation, greater amounts of estrogen or vitamin D deficiency. Obese men and women had a 24 percent increased risk of developing RA. The researchers are worried, since the prevalence of obesity in the general population continues to rise. This is not good news on the whole; women are more likely than men to develop RA, in general, according to a separate study (Ann Rheum Dis. 2007;66:1491-1496).

Obesity results in less robust outcomes when it comes to RA treatment. In an abstract presented at the European League Against Rheumatism Congress 2013, those who were obese had a two-fold greater risk of being on TNF (tumor necrosis factor) alpha inhibitors, compared to those who were of normal weight (BMI <25 kg/m2) (EULAR Congress 2013 Abstract OP0178). The researchers treated 346 RA patients with methotrexate plus or minus prednisone, but if they did not respond sufficiently, a TNF alpha inhibitor was added.

This occurred significantly more frequently with obese patients. Those who were obese had a less-than-ideal response to methotrexate plus or minus prednisone at a rate that was more than two times greater at 12 months than those of normal weight. Again, inflammation was postulated as the potential cause of poor response to the initial treatment in obese patients.

In yet another study, obese patients’ response to TNF alpha inhibitors was less robust compared to those who were not obese (Arthritis Care Res (Hoboken). 2013 Jan;65(1):94-100). At the end of the first year, remission rates of RA in obese patients were less than half those of normal patients. However, when the researchers analyzed the individual TNF alpha inhibitors, only Remicade’s (infliximab) poor response reached statistical significance, while the others were trending toward significance. This study involved 641 patients, but only 66 who were obese.

Let’s recap: patients with a history of obesity are twice as likely to develop RA and require TNF alpha inhibitors, but the effectiveness of these TNF inhibitors is reduced for them.

Lifestyle modifications

Lifestyle changes are critical to treating obesity; however, not all lifestyle modifications, including diet and exercise, are created equal. A recent study showed that those on a very low-calorie diet, or “crash diet,” were three times more likely to develop gallstones than those on a low-calorie diet (Int J Obes (Lond). Online 2013;May 22). The participants on the very low-calorie approach consumed liquid meals for 6 to 10 weeks, ingesting 500 calories per day, and then switched to a maintenance diet. The low-calorie group consumed liquid meals and solid foods totaling 1,200 to 1,500 calories per day for 12 weeks and then switched to a maintenance diet.

The reason for increased gallstones may be the impact of a very low-calorie diet on the bile’s composition and the gallbladder’s ability to discharge it. There were over 6,000 participants involved in the study. Thus, losing weight too rapidly is probably not the best approach.

In my experience, a high-nutrient, plant-based diet is one effective method for losing weight. I wrote about the quality of calories consumed, mindful eating and exercise in two articles published on Aug. 2, 2012 and April 30, 2013. I encourage you to read them, if you want to learn more about this topic.

Whether or not you agree with the AMA’s decision to elevate obesity to a chronic disease, it needs to be treated. Lifestyle modifications should be included in every paradigm, regardless of whether surgery or drugs are used as well. Some people may benefit from drug therapy, and some may benefit from surgery, but all will benefit from appropriate lifestyle modifications.

Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management. For further information, go to the website www.medicalcompassmd.com or consult your personal physician.

Rheumatoid arthritis is a complicated autoimmune disease to manage, especially in the more advanced stages. It is important that we stay abreast of the latest research, since RA is becoming more common (Arthritis Rheum. 2010 June;62(6):1576-1582). Recently, the prestigious European League Against Rheumatism (EULAR) Congress 2013 had its annual conference, so I thought it appropriate to discuss some of the findings. Most of the data is in abstract form and considered preliminary until the papers are fully published.

RA can be one of the most disabling diseases, with symptoms such as morning stiffness, diffuse joint pain and swelling that can affect multiple joints, with the proximal joints in the hands, wrists and feet most commonly affected bilaterally (Lancet. 2001;358(9285):903-911). It is not uncommon for RA patients also to be depressed, which can take its toll on productivity.

Treatment options

Medications used to treat RA involve disease-modifying antirheumatic drugs. One of the most common drugs used is methotrexate, which is frequently combined with tumor necrosis factors alpha inhibitors, such as Remicade (infliximab), Enbrel (etanercept), Humira (adalimumab) and other DMARDs. We will discuss the benefits and drawbacks of TNF inhibitors, which have anti-inflammatory effects, but also suppress the immune system.

The goal of these drugs is to reduce synovitis, or inflammation in the joints, helping to lessen joint damage. They can be quite effective. Unfortunately, compliance can be an issue. Nonsteroidal anti-inflammatory drugs (NSAIDs) are also used for treatment, however, they should not be combined with methotrexate or at least caution should be advised when doing so.

Lifestyle modifications may also play a role in ameliorating RA, including helping with fall risk.

Compliance

Even though there are a number of drug therapy options, compliance is an issue. In a recent study, approximately 33 percent of patients stopped or switched their RA medication within the first year, and by year two, the number increased to approximately half of patients (EULAR, Abstract OP0064). Patients on TNF inhibitors discontinued slightly less.

The main reason for discontinuation was a perceived lack of drug effectiveness, followed by side effects and therapy preferences. For those on TNF inhibitors, adverse reactions or safety were the main concerns. The greater the symptoms and progression of the disease, and the higher the psychological toll of the disease, such as depression and anxiety, the higher the probability that medication would be discontinued.

There were over 6,000 RA patients involved in this study, with disease duration averaging 11 years. The researchers used the Consortium of Rheumatology Researchers of North America registry to make this assessment.

FDA warning

Why might side effects be a concern for TNF inhibitors? In 2011, the FDA found there were 100 cases of Listeria and Legionella pneumonia infections associated with these drugs. Therefore, a warning was placed on all TNF inhibitors. The median duration that patients were on the drugs when they experienced infections was about 10 months. However, most patients were also on methotrexate and steroids at the time of infection.

While there were infections that took place during these drugs’ clinical trials, the absolute number was small. There was a large, though retrospective, study suggesting that the risk of serious infections requiring hospitalization is not greater than with other RA medications (JAMA. 2011;306:2331-2339).

Head-to-head trial of DMARDs or biologics

There was a recent head-to-head, blinded, randomized controlled trial, called the AMPLE trial, comparing two different types of DMARDs, Humira (adalimumab), a TNF inhibitor, and Orencia (abatacept), a non-TNF inhibitor (EULAR: Abstract OP0044). Both medications showed equivalent results in RA and are popular therapies for patients who have moderate to severe disease. Radiographic tests showed no joint damage progression in 85 percent of patients. However, there were fewer side effects with Orencia. Why is this important? Because if a patient can’t tolerate one drug, or if it does not work for them, then they can be confident that there are other, equally effective, options. This trial was two years in duration and involved 643 patients.

Depression

In one study, results showed that patients with early RA were more likely to apply for disability and subsequent early retirement due to depression than from symptoms of the disease, the level of work stress, other disease in combination with RA or the perceived effectiveness of drug therapy (EULAR: Abstract OP0092). Within the first year of being diagnosed with RA, depression outweighed other factors as a reason for disability by more than threefold.

The authors suggest that a questionnaire could help identify depressed patients so they could be treated appropriately, potentially preventing disability and early retirement. There were 563 patients involved in this study.

Falls

In a recent study involving 535 patients, results showed that RA patients have a greater probability of repeat falls (Arthritis Care Res. Online 2013 Feb. 22). This may not be surprising, considering the symptoms of joint stiffness, pain and swelling. The greatest predictor of future falls was a fall history. Therefore, patients with RA need to be asked about their tendency to fall. After the first fall, patients were three times as likely to fall again. Though history of fall was most valuable, symptoms of the disease, such as swollen joints and pain were also important. Interestingly, medications for treating depression contribute to fall risk. As we mentioned, RA patients have a higher tendency to be depressed. So what can be done to reduce fall risk? Lifestyle modifications with tai chi may be one option.

Lifestyle modifications

Lifestyle modifications include tai chi, diet, fish oil and aerobic exercise. I wrote about fish oil and aerobic exercise in my April 19, 2012, article entitled, “Rheumatoid arthritis effective management options.”

There was an extensive systematic review of the literature, which demonstrated that tai chi may have a role in reducing the risk of falls in RA by strengthening muscles and increasing flexibility (Br J Sports Med. 2012 Aug.;46(10):713-718). Unfortunately, tai chi did not have any effect on RA patients’ symptoms.

Since rheumatoid arthritis can be such a debilitating disease, both physically and mentally, it requires a significant partnership by the patient and doctor to treat it with medication and lifestyle modifications.

Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management. For further information, go to the website www.medicalcompassmd.com and consult your personal physician.

Heart attacks and heart disease get a lot of attention, but chronic heart failure is something that tends to be overlooked by the press. Heart failure occurs in about 20 percent of the population over the age of 40 (Circulation. 2002;106(24):3068). There are about 5.8 million Americans with HF (Circulation. 2010;121(7):e46). Not surprisingly, incidence of heart failure increases with age (J Am Coll Cardiol. 2003;41(2):21).

Heart failure occurs when the heart’s pumping is not able to keep up with the body’s demands and may decompensate. It is a complicated topic, for there are two types, systolic heart failure and diastolic heart failure. The basic difference is that the ejection fraction (output of blood with each contraction of the left ventricle of the heart) is more or less preserved in diastolic HF, while it can be significantly reduced in systolic HF.

We have more evidence-based medicine, or medical research, on systolic heart failure. Fortunately, both types can be diagnosed with the help of an echocardiogram, an ultrasound of the heart. The signs and symptoms may be similar, as well, and include shortness of breath on exertion or when lying down; edema or swelling; reduced exercise tolerance; weakness and fatigue. The risk factors for heart failure include diabetes, coronary artery disease, high blood pressure, obesity, smoking, heart attacks and valvular disease.

Typically, heart failure is treated with blood pressure medications, such as beta blockers, ACE inhibitors and angiotensin receptor blockers.

We are going to look at how diet, iron and the supplement CoQ10 impact heart failure.

Effect of diet

If we look beyond the usual risk factors mentioned above, oxidative stress may play an important role as a contributor to HF. Oxidative stress is thought to potentially result in damage to the inner lining of the blood vessels, or endothelium, oxidation of cholesterol molecules, and a decrease in nitric oxide, which helps vasodilate blood vessels.

In a newly published population-based, prospective (forward-looking) study, called the Swedish Mammography Cohort, results show that a diet rich in antioxidants reduces the risk of developing HF (Am J Med. 2013 Jun:126(6):494-500) In the group that consumed the most nutrient-dense foods, there was a significant 42 percent (p<0.001) reduction in the development of HF, compared to the group that consumed the least. According to the authors, the antioxidants were derived mainly from fruits, vegetables, whole grains, coffee and chocolate. Fruits and vegetables were responsible for the majority of the effect.

This nutrient-dense approach to diet increased oxygen radical absorption capacity. Oxygen radicals have been implicated in cellular damage and DNA damage, potentially as a result of increasing chronic inflammation. What makes this study so impressive is that it is the first of its kind to investigate antioxidants from the diet and their impacts on heart failure prevention. This was a large study, involving 33,713 women, with good duration — follow-up was 11.3 years. There are limitations to this study, since it is an observational study, and the population involved only women. Still, the results are very exciting, and it is unlikely there is a downside to applying this approach to the population at large.

CoQ10 supplementation

Coenzyme Q 10 is a substance produced by the body that helps the mitochondria (the powerhouse of the cell) produce energy. It is thought of as an antioxidant. In a meta-analysis (group of 13 studies), the results showed that supplementation with CoQ10 may help improve functioning in patients with heart failure (Am J Clin Nutr. 2013 Feb;97(2):268-75). This may occur because of a modest rise in ejection fraction functioning. It seems to be important in systolic heart failure. Supplementation with CoQ10 may help to reduce its severity.

The doses used in the meta-analysis ranged from 60 mg to 300 mg. Interestingly, those that were less than or equal to 100 mg showed statistical significance, while higher doses did not reach statistical significance. This CoQ10 meta-analysis was small. It covered 13 studies and fewer than 300 patients.

Like some other supplements, CoQ10 has potential benefits, but more study is needed. Because there are no studies showing significant deleterious effects, which doesn’t mean there won’t be, it is worth starting HF patients with comprised ejection fractions on 100 mg CoQ10 and titrating up, as long as patients can tolerate it.

Preliminary results of the new Q-SYMBIO study showed an almost 50 percent reduction in the risk of all-cause mortality and 50 percent fewer cardiac events with CoQ10 supplementation. This one randomized controlled trial followed 420 patients for two years who had severe heart failure.

The lead author goes as far as to suggest that CoQ10 should be part of the paradigm of treatment. He may be a bit enthusiastic, but this is the first new “drug” in over a decade to show survival benefits. The caveat is that these results were only recently presented at the prestigious Heart Failure 2013 Congress May 25 to 28, and they still need to be published in a peer-reviewed journal.

Iron Deficiency

Anemia and iron deficiency are not synonymous, since iron deficiency can occur without anemia. A recent observational study that followed 753 heart failure patients for almost two years showed that iron deficiency without anemia increased the risk of mortality in heart failure patients by 42 percent (Am Heart J. 2013;165(4):575-582).

In this study, iron deficiency was defined as a ferritin level less than 100 ug/L (the storage of iron) or, alternately, transferrin saturation less than 20 percent (the transport of iron) with a ferritin level in the range 100-299 ug/L.

The authors conclude that iron deficiency is potentially more predictive of clinical outcomes than anemia, contributes to the severity of HF, and is common in these patients.

Thus, it behooves us to try to prevent heart failure through dietary changes, including high levels of antioxidants, because it is not easy to reverse the disease. Those with HF should have their ferritin levels checked, for these are correctable. I am not typically a supplement advocate; however, based on the latest results, CoQ10 seems like a compelling therapy to reduce risk of further complications and potentially death. Consult with your doctor before taking CoQ10 or any other supplements, especially if you have heart failure.

Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management. For further information, go to the website www.medicalcompassmd.com or consult your personal physician.

Sodium is once again mired in controversy. The Institute of Medicine recently released a report that questioned the levels to which Americans should reduce their sodium levels in order to reduce chronic ailments, such as cardiovascular disease. Interestingly, the IOM and the American Heart Association disagree. The AHA believes stricter levels are critically important.

The generally accepted guidelines suggest that healthy people reduce their daily sodium intake to less than 2,300 milligrams, or about a teaspoon, and that those in high-risk categories reduce this further to less than 1,500 mg, or just over a half teaspoon. About 70 percent of Americans are at high risk, which includes those over 50, African Americans and patients with chronic kidney disease, heart failure, diabetes, hypertension (high blood pressure) or prehypertension (MMWR Morb Mortal Wkly Rep 2009; 58:281-283).

The IOM was asked to determine whether there was enough information to suggest everyone follow the less-than-1,500-mg sodium levels, regardless of their risk level. However, the IOM did not find enough data to substantiate that level and even questioned whether 2,300 mg may be too low. If the IOM is right and the research does not support less than 1,500 mg of sodium for anyone, should we be more liberal with sodium? The short answer is “No.”

We will discuss an article written by The New York Times, the Center for Science in the Public Interest’s response and the beneficial effects of sodium reduction on dementia.

The New York Times

On May 14, NYT published an article on the IOM’s findings. NYT did say that IOM showed inconclusive results as to whether levels less than 1,500 mg daily are beneficial or not. However, NYT went further, suggesting sodium levels less than 1,500 mg may be dangerous to your health.

The author of the article referenced two studies. The first is a small, randomized controlled Italian study of patients with moderate to severe congestive heart failure. It showed those who consumed 1,840 mg of sodium per day were about three times as likely to be readmitted to the hospital and about twice as likely to suffer mortality, compared to those who consumed more sodium, 2,760 mg per day (Clin Sci (Lond). 2008 Feb;114(3):221-30).

In the second study, an observational one, patients with high blood pressure who consumed more than 7,000 mg of sodium or who consumed less than 3,000 mg per day were more likely to have cardiovascular events, such as congestive heart failure, heart attacks and stroke, as well as higher risk of death (JAMA. 2011 Nov 23;306(20):2229-38). The results are what researchers call a J curve, where the patients at the extremes suffer, while those in the middle do better.

Center for Science in the Public Interest

What are we to make of the studies? Even though The New York Times is one of the most prominent newspapers in the country, it is not a peer-reviewed medical journal and, in this case, the journalist is not a scientist.

However, there was an intriguing response from Michael F. Jacobson, who has a doctorate in microbiology from MIT and is the executive director of the CSPI, a highly regarded nonprofit organization focused on health and science. In his analysis of the NYT article and the IOM findings, he found several problems. The New York Times did not bring to light the fact that the IOM report found the evidence of a detrimental effect from very low sodium levels in the diet was “insufficient and inconsistent.” In other words, no conclusion could be drawn.

The studies that showed dangerous effects with very low sodium, including those mentioned above, were flawed in their methodology. It also included a strange treatment regimen for the congestive heart failure patients in the Italian study because they were restricted not only with sodium levels but also significantly limiting the amount of water intake, which is not something we typically do in the U.S. In addition, according to “National Health and Nutrition Examination Survey” data from 2003 to 2006, less than 5 percent of Americans actually consume strict sodium levels of less than 1,500 mg (ars.usda.gov). Jacobson points out that the IOM also did not take into account that consuming less sodium results in lower blood pressure.

As we know, high blood pressure leads to cardiovascular disease and potentially increased mortality. This is why the AHA believes that a sodium intake of less than 1.500 mg is so important, not just for high-risk patients, but also for the general population (www.heart.org/sodium). In the Trials of Hypertension Prevention follow-up, the results showed that a 25 percent reduction of sodium from 3,556 mg to 2,286 mg daily results in a 25 to 30 percent reduction in cardiovascular events, including heart attacks and strokes (BMJ 2007;334:885). This was one of the few studies the IOM said was not flawed.

So how are Americans doing? Not very well. We are currently consuming an average of 3,463 mg per day as of 2010 (www.heart.org/sodium). Evidence shows that the restaurant industry is contributing to Americans’ consumption of higher sodium (JAMA Intern Med online 2013;May 13). From 2005 to 2011, the amount of sodium used by the industry increased. Many processed foods are also part of the problem.

Preventing cognitive decline in older adults

With sedentary older adults (67 to 84 years old), a relatively recent population study showed that those who consumed less sodium had a lower risk of cognitive decline in a linear relationship (Neurobiol Aging 2012;33(4):829.e21-829.e28). Those who consumed the lowest levels (about 1,800 mg) of sodium saw less decline than those consuming higher levels (approximately 2,600 mg and 3,900 mg). It was an intake-dependent response. Interestingly, those who exercised regularly were not affected by sodium levels.

Sodium reduction may be important for additional diseases, such as osteoporosis and kidney stones. I wrote about the beneficial effects of reduced sodium on May 25, 2011.

The IOM and the CSPI make a strong case that there does not seem to be any downside to lowering sodium especially since we get far too much in our diet. Sodium reduction is a simple way of lowering the risk of cardiovascular disease and events, as well as potentially other chronic diseases. And the good news is that our taste buds usually adapt to lower sodium levels within six weeks, making food taste more vibrant.

Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management. For further information, go to the website www.medicalcompassmd.com or consult your personal physician.

“White-coat hypertension” (high blood pressure) is defined as blood pressure that is elevated to at least 140/90 mm Hg at a physician’s office, but “normal” when measured at home. The blood pressure considered normal at home is less than 135/85 mm Hg. This is a real phenomenon caused by the anxiety or stress of being in a doctor’s office. It is also known as “isolated office hypertension.”

About 20 to 30 percent of patients experience white-coat hypertension (www.uptodate.com). However, when the diastolic (bottom number) blood pressure is greater than 105 mm Hg, it is unlikely to be simply caused by doctor’s office-related stress (J Hypertens. 2001;19(6):1015).

Consequences

What are the consequences of white-coat hypertension? We sometimes discount it, because it seems benign or harmless. However, some studies show that it may increase the risk of sustained hypertension, which is a major contributor to developing cardiovascular disease — heart disease and stroke.

It is very important to take white-coat hypertension seriously, because recent data shows that hypertension rose by 10 percent in the United States in the four years from 2005 to 2009 (CDC.gov).

What can be done?

What can be done about white-coat hypertension? Well, it does not need to be treated with medication, except potentially in elderly patients (over 80 years of age), but should involve lifestyle modifications, including dietary changes, stress reduction and exercise. In terms of diet, increased beet juice, green leafy vegetables and potassium, as well as decreased sodium intake may be important. You should monitor the blood pressure at home, taking multiple readings during the day, or by 24-hour ambulatory blood pressure readings, which require wearing a monitor. The latter provides the additional advantage of blood pressure readings during your sleep.

If you do monitor your blood pressure at home, the American Heart Association has suggestions on how to get the most accurate readings, such as measurements early in the morning before exercising and eating, as well as in the evening (Am Fam Physician. 2005 Oct 1;72(7):1391-1398). You should also be comfortably seated, don’t cross your legs and sit for a few minutes before taking a reading. For more details, see the article referenced, which was published in the American Family Physician journal. Let’s look at the evidence.

Risk of sustained high blood pressure

There were no substantial studies demonstrating any consequences from white-coat hypertension until 2005. Most previous studies on white-coat hypertension were not of long enough duration.

In the 2005 population-based Ohasama study, results showed that the participants who had white-coat hypertension were 2.9 times more likely to develop sustained hypertension, compared to those who had normal blood pressure in the doctor’s office (Arch Intern Med. 2005 Jul 11;165(13):1541-6). There were almost 800 participants involved in this study, with a mean age at the start of 56. What was really impressive about the study was its duration, with an eight-year follow-up. This gives a better sense of whether white-coat hypertension may develop into sustained hypertension. The researchers concluded that it may lead to a less than stellar outlook for cardiovascular prognosis.

Another study, published in 2009, reinforced these results. The PAMELA study showed that those with white-coat hypertension had about a 2.5-times increased risk of developing sustained high blood pressure, compared to those who had normal readings in all environments (Hypertension. 2009; 54: 226-232). There were 1,412 participants involved in the study, ranging in age from 25 to 74. Just like the previous study, an impressive aspect was the fact that there was a long follow-up period of 10 years. Thus, this was a substantial study, applicable to the general population over a significant duration.

Prevention of sustained hypertension

In a recent small, randomized controlled trial, beet juice was shown to reduce blood pressure significantly (Hypertension. Online 2013; April 15). Patients either were given 250 ml (about 8 ounces) of beet juice or comparable amounts of water. The patients who drank the beet juice saw an 11.2 mm Hg decrease in blood pressure, while those who drank water saw a 0.7 mm Hg reduction. This effect with the beet juice continued to remain significant. Even after 24 hours, there was a sustainable 7.2 mm Hg drop in blood pressure, compared to readings taken prior to drinking the juice.

Though these results are encouraging, we need to study whether these effects can be sustained over the long term with daily beet juice consumption. Also, this study was done in patients with high blood pressure. I don’t know of any prevention studies done in patients with white-coat hypertension.

The researchers believe the effect is caused by high nitrate levels in beet juice that are converted to nitrite when it comes in contact with human saliva. Nitrite helps to vasodilate, or enlarge blood vessels, and thus helps to decrease blood pressure in a similar way as some antihypertensive (blood pressure) medications.

The authors go on to surmise that green leafy vegetables offer protection from cardiovascular disease in part due to increased nitrite levels, similar to those in beet juice. If you have diabetes, prediabetes, a family history or a high risk for diabetes, I recommend eating beets instead, since drinking beet juice will raise your sugar levels.

Increasing potassium levels significantly through food sources, not supplements, has a profound effect in reducing blood pressure. In a study where 3,500 to 4,700 mg of potassium were consumed through foods, the systolic (top number) blood pressure was reduced by 7.1 mm Hg (BMJ. 2013 Apr 3;346:f1378). We should be getting 4,700 mg of potassium daily, which equates to about 10 bananas daily. Almonds, raisins and green leafy vegetables, such as Swiss chard, also have significant amounts of potassium. To learn more about potassium’s effect on blood pressure, please read my April 11, 2013 article.

White-coat hypertension should not be neglected. It is important to monitor blood pressure at home for at least three days with multiple readings, and then send them to your physician for review. Though patients don’t need to be on blood pressure medications at this stage, it does not mean you should be passive about the process. Make lifestyle modifications to reduce your risk of developing sustained hypertension.

Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management. For further information, go to the website www.medicalcompassmd.com and/or consult your personal physician.

Everyone has a heart rate, so everyone needs to pay attention. But what does that heart rate, or pulse, tell us beyond the obvious fact that we are alive?

Our “normal” resting heart rate is between 60 to 100 beats per minute. We know that a RHR above 100 bpm is abnormal; it is referred to as tachycardia, or a racing heartbeat, and has potentially serious consequences. However, even “normal” RHRs can be stratified to identify risks for diseases. What I mean is that, even in the “normal” range, as your resting heart rate increases, so do your potential risks. Actually, RHR below approximately 70 bpm may be ideal.

The importance of the resting heart rate should not be underestimated. In fact, it may play a role in longevity, heart disease — including heart failure, arrhythmias, heart attacks and sudden cardiac death, and even chronic kidney disease.

The good news is that the RHR is modifiable. Methods that may reduce your rate include medications for high blood pressure, such as beta blockers and lifestyle modifications, including meditation, dietary changes and exercise.

Impact on lifespan

We all want to live longer and healthier lives. Reducing the RHR may be an important component in achieving this goal.

In the Copenhagen Male Study, a prospective (forward-looking) study that followed 2,798 participants for 16 years, results showed that those with higher resting heart rates had greater risk of death (Heart Journal 2013 Jun;99(12):882-7). There was a linear relationship between risk of death and increasing RHR. Those who had a resting heart rate above 90 bpm were at a threefold greater risk of death, compared to those who had a RHR at or below 50 bpm. RHR was inversely related to the amount of physical activity.

Thus, the authors concluded that a “healthy” person with higher RHR may still have a shorter lifespan, with all other factors being equal, such as physical activity and blood pressure.

In contrast with the previous study, the following one took a “glass is half-full approach” to longevity. The Jerusalem longitudinal cohort study showed that elderly women and men who had a lower RHR lived the longest (J Am Geriatr Soc. 2013;61(1):40-45). There were more than 2,000 participants, ranging from 70 to 90 years old.

Heart disease mortality

In the Nord-Trondelag health study, a prospective observational study, those with a higher RHR at the end of the study than they did 10 years prior, at the beginning of the study, were more likely to die from heart disease (JAMA 2011; 306:2579-2587). In other words as the RHR increased from less than 70 bpm to over 85 bpm, there was a 90 percent greater risk of heart disease, compared to those who maintained a RHR of less than 70 throughout the two measurements. This study involved 30,000 participants, but unlike some other studies, many of us can relate to the population: They were at least 20 years old and were healthy volunteers.

Heart attacks

It is more common for women to have heart attacks with atypical symptoms than men. Therefore, it is very important for women to reduce their risks. In the Women’s Health Initiative, results showed a 26 percent decrease in the risk of cardiovascular events in those postmenopausal who had a RHR below 62 bpm, compared to those who had a RHR above 76 bpm (BMJ. 2009 Feb 3;338:b219). Interestingly, these results were even more substantial in the subgroup of women who were newly postmenopausal, ranging in age from 50 to 64.

Effect on kidney function

Since I wrote about chronic kidney disease on May 9, I thought an interesting follow-up might be resting heart rate and its impact on kidney function. In the Atherosclerosis Risk in Communities Study, results showed that the most severe form of chronic kidney disease, end-stage renal disease, was 98 percent more likely to occur in those with the highest RHR, compared to those with the lowest (J Am Soc Nephrol. 2010 Sep;21(9):1560-70). There were approximately 13,000 participants in the study, with a 16-year follow-up.

The authors hypothesized that this negative affect on the kidney may be due to a loss of homeostasis in the autonomic (involuntary) nervous system, resulting blood vessel dysfunction, such as increased inflammation and vasoconstriction (narrowing).

Eating fish

What can be done to reduce the resting heart rate with minimal side effects? Fish consumption has recently been shown to have a positive effect. In a study, European men who ate greater amounts of fish — more than one serving per week — had lower resting heart rates than those who ate fish rarely (Circulation. 2003;108:820-825). There was also a direct relationship between the amount of fish consumed and the RHR: The more fish consumed per week, the greater the reduction in RHR. This was a prospective observational study involving about 5,000 men. Some beneficial side effects of eating fish included decreased triglycerides and diastolic (lower number) blood pressure, as well as increased HDL (“good cholesterol”). Even after controlling for these beneficial side effects, there still was a significant improvement in RHR with fish consumption.

Is there a resting heart rate that is too low? Well, it depends on the context. If you are a marathoner or an athlete, then a RHR in the 40s may not be abnormal. For a healthy, physically active individual, it is not uncommon to have a resting heart rate in the 50s. However, if you are on medications that reduce your RHR and/or have a chronic disease, such as heart failure, it is probably not advisable to go much below 60 bpm. Always ask your doctor about the appropriate resting heart rate for your particular situation.

Thus, resting heart rate is an easy and inexpensive biomarker to potentially determine risk stratification for disease manifestation and to increase longevity, even for those in the “normal” range. We can utilize RHR as tool for primary prevention of disease. The fact that it is modifiable means it is something that we need to monitor, so that we can achieve the ideal RHR, rather than just the “normal.”

Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management. For further information, go to the website www.medicalcompassmd.com and/or consult your personal physician.

Chronic kidney disease is on the rise in this country. In a study that looked at data from the National Health and Nutrition Examination Survey, prevalence of chronic kidney disease (CKD) increased more than 30 percent from 1988 to 2004 (JAMA. 2007;298:2038-2047). Early-stage (mild) CKD is no exception and may not be getting enough attention. In this article, we will look beyond the more obvious causes of mild chronic kidney disease, such as diabetes, smoking, aging, obesity and high blood pressure (JAMA. 2004;291:844-850).

Why is early-stage CKD so important? It is associated with a 40 percent increased risk of developing cardiovascular events, such as heart attacks (N Engl J Med. 2004;351:1296-1305). It also significantly increases the risk of peripheral artery disease (PAD). Those with decreased kidney function have a 24 percent prevalence of PAD, compared to 3.7 percent in those with normal kidney function (Circulation. 2004;109:320–323). Of course, it can lead ultimately to end-stage renal (kidney) disease, requiring dialysis and potentially a kidney transplant.

One of the problems with early-stage CKD is that it tends to be asymptomatic. However, there are simple tests, such as a basic metabolic panel and a urinalysis, that will indicate whether a patient may have mild chronic kidney disease. These indices for kidney function include an estimated glomerular filtration rate (eGFR), creatinine level and protein in the urine. While the other two indices have varying ranges depending on the laboratory used, a patient with an eGFR of 30 to 59 mL/minute/1.73 m2 is considered to have mild disease. The eGFR and the kidney function are inversely related, meaning as eGFR declines, the more severe the chronic kidney disease.

What can be done to stem early-stage CKD, before complications occur? There are several studies that have looked at medications and lifestyle modifications and their impacts on its prevention, treatment and reversal.

Let’s look at the evidence.

Medications

Allopurinol is usually thought of as a medication for the prevention of gout. However, in a randomized controlled trial, the gold standard of studies, the results show that allopurinol may help to slow the progression of CKD, defined in this study as an eGFR less than 60 mL/min/1.73 m2 (Clin J Am Soc Nephrol. 2010 Aug;5:1388-1393). The group using 100 mg of allopurinol showed significant improvement in eGFR levels (a 1.3 mL/minute per 1.73 m2 increase) compared to the control group (a 3.3 mL/minute per 1.73 m2 decrease) over a two-year period. There were 113 patients involved in this study. The researchers concluded that there was a slow progression of CKD with allopurinol. Allopurinol also decreased cardiovascular risk by 71 percent.

Fibrates are a class of drug usually used to boost HDL (“good”) cholesterol levels and reduce triglyceride levels, another cholesterol marker. Fibrates have gotten negative press recently for not showing improvement in cardiovascular outcomes. However, in patients with mild to moderate CKD, a meta-analysis (a group of 10 studies) recently showed a 30 percent reduction in major cardiovascular events and a 40 percent reduction in the risk of cardiovascular mortality with the use of fibrates (J Am Coll Cardiol. 2012 Nov. 13;60:2061-2071). This is important, since patients with CKD are mostly likely to die of cardiovascular disease.

The authors concluded that fibrates seem to have a much more powerful beneficial effect in CKD patients, as opposed to the general population. So, there may be a role for fibrates after all.

Lifestyle modifications

Fruits and vegetables may play a role in helping patients with CKD. In a recent study, the results showed that fruits and vegetables work as well as sodium bicarbonate in improving kidney function by reducing metabolic acidosis levels (Clin J Am Soc Nephrol. 2013;8:371-381).

What is the significance of metabolic acidosis? It means that body fluids become acidic and it is associated with chronic kidney disease. The authors concluded that both sodium bicarbonate and a diet including fruits and vegetables were renoprotective, helping to protect the kidneys from further damage in patients with CKD. Alkali diets are primarily plant-based, although not necessarily vegetarian or vegan-based diets. Animal products tend to cause an acidic environment. The study was one year in duration, however, though the results were impressive, the study was small, with 77 patients.

Sodium rears its ugly head yet again. Red meat is not thought of positively, and animal fat is not far behind. In the Nurses’ Health Study, the results show that animal fat, red meat and salt all negatively impact kidney function (Clin J Am Soc Nephrol. 2010; 5:836-843). The risk of protein in the urine, a potential indicator of CKD, increased by 72 percent in those participants who consumed the highest amounts of animal fat compared to the lowest, and by 51 percent in those who ate red meat at least twice a week. With higher amounts of sodium, there was a 52 percent increased risk of having lower levels of eGFR.

The most interesting part with sodium was that the difference between higher mean consumption and the lower mean consumption was not that large, 2.4 grams compared to 1.7 grams. In other words, the difference between approximately a teaspoon of sodium and three quarters of a teaspoon was responsible for the decrease in kidney function.

In my practice, when CKD patients follow a vegetable-rich, nutrient-dense diet, there are substantial improvements in kidney functioning. For instance, for a recent patient, his baseline eGFR was 54 mL/min/1.73 m2. After one month of lifestyle modifications, his eGFR improved by 9 points to 63 mL/min/1.73 m2, which is a return to “normal” functioning of the kidney. However, this is an anecdotal story and not a study.

Therefore, it is important to have your kidney function checked with mainstream tests. If the levels are low, we should address the issue through medications and/or lifestyle modifications to manage and reverse early-stage CKD. However, lifestyle modifications don’t have the negative side effects of medications. Don’t wait until symptoms and complications occur. In my experience, it is much easier to treat and reverse a disease in its earlier stages, and CKD is no exception.

Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management. For further information, go to the website www.medicalcompassmd.com and/or consult your personal physician.

When we think of losing weight, calories are usually the first thing that comes to mind. We know that the more calories we consume, the greater our risk of becoming overweight or obese and developing many chronic diseases, including top killers such as heart disease, diabetes and cancer. Despite this awareness, obesity and chronic diseases are on the rise according to the Centers for Disease Control.

How can this be the case? I am usually focused on the quality of foods, rather than calories, and I will delve into this area as well, but we suffer from misconceptions and lack of awareness when it comes to calories. The minefield of calories needs to be placed in context. In this article, we will put calories into context, as they relate to exercise, and help to elucidate the effects of mindful and distracted eating.

Let’s look at the studies.

Impact of energy expenditure

One of the most common misconceptions is that if we exercise, we can be more lax with what we are eating. But researchers in a recent study found that this was not the case (J Exp Biol. 2013; Abstract 367.2). The results showed that when menu items were associated with exercise expenditures, consumers tended to make better choices and ultimately eat fewer calories. In other words, including the amount of exercise needed to burn calories was paired on the menu with food options, resulting in a significant reduction in overall consumption. The example that the authors gave was that of a four-ounce cheeseburger, which required that women walk with alacrity for two hours in order to burn off the calories.

Those study participants who had menus and exercise expenditure data provided simultaneously, compared to those who did not have the exercise data, chose items that resulted in a reduction of approximately 140 calories, 763 versus 902 kcals.

Even more interestingly, study participants not only picked lower calorie items, but they ate less of those items. Although this was a small preliminary study, the results were quite impactful. The effect is that calories become a conscious decision rooted in context, rather than an abstract choice.

The importance of mindful eating

Most of like to think we are multitaskers. However, when eating, multitasking may be a hazard. In a meta-analysis (a group of 24 studies), researchers found that when participants were distracted while eating, they consumed significantly more calories immediately during this time period, regardless of dietary constraints (Am J Clin Nutr. 2013 April;97:728-742).

This distracted eating also had an impact on subsequent meals, increasing the amount of food eaten at a later time period, while attentive eating reduced calories eaten in subsequent meals by approximately 10 percent. Distracted eating resulted in greater than 25 percent more calories consumed for the day. When participants were cognizant of the amount of food they were consuming, and when they later summoned memories of their previous eating, there was a vast improvement in this process.

The authors concluded that reducing distracted eating may be a method to help in both weight loss and weight management, providing an approach that does not necessitate calorie counting. These results are encouraging, since calorie counting frustrates many who are watching their weight over the long term.

The perils of eating out

Most of us eat out at least once in a while. In many cultures, it is a way to socialize. However, as much as we would like to control what goes into our food, we lose that control when eating out. In a study that focused on children, the results showed that when they ate out, they consumed more calories, especially from fats and sugars (JAMA Pediatr. 2013;167:14-20). Of the 9,000 teenagers involved in the study, between 24 percent and 42 percent had gone to a fast food establishment and 7 to 18 percent had eaten in sit-down restaurants when asked about 24-hour recall of their diets on two separate occasions.

Researchers calculated that this resulted in increases of 310 calories and 267 calories from fast food and sit-down restaurants, respectively. This is not to say we shouldn’t eat out or that children should not eat out, but that we should have more awareness of the impact of our food choices. For example, the Bloomberg administration has required calories be displayed in many New York City chain restaurants.

Quality of calories

It is important to be aware of the calories we are consuming, not only from the quantitative perspective, but also from a perspective that includes the quality of those calories. In another study involving children, the results showed that those offered vegetables for snacks during the time that they were watching television needed significantly fewer calories to become satiated than when given potato chips (Pediatrics. 2013;131:22-29). The authors commented that this was true for overweight and obese children as well, however, they were more likely to be offered unhealthy snacks, like potato chips.

In a paper published in JAMA in June 2012, the authors state that we should not restrict one type of nutrient over another, but rather focus on quality of nutrients consumed (JAMA 2012; 307:2627-2634).

In my practice, I find that when my patients follow a vegetable-rich, nutrient-dense diet, one of the wonderful “side effects” they experience is a reduction or complete suppression of food cravings. As far as mindless eating goes, I suggest if you are going to snack while working, watching TV or doing some other activity, then snack on a nutrient-dense, low-calorie food, such as carrots or blackberries. If you don’t remember how many vegetables or berries that you ate, you can take heart in knowing it’s beneficial. It can also be helpful to keep a log of what you’ve eaten for the day, to increase your cognizance of distracted eating.

Therefore, rather than counting calories and becoming frustrated by the process, be aware of the impact of your food choices. Why not get the most benefit out of lifestyle modifications with the least amount of effort? Rather than having to exercise more to try to compensate, if you actively choose nutrient-dense, low-calorie foods, the goal of maintaining or losing weight, as well as preventing or potentially reversing chronic diseases, becomes attainable through a much less painful and laborious process.

Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management. For further information, go to the website www.medicalcompassmd.com and/or consult your personal physician.

L-carnitine, or carnitine, has been around for a while. The people most familiar with it may be athletes, because for years it has been touted as possibly providing more energy, though the research has not borne out on this topic.

What is L-carnitine and why is it of interest? It is derived from amino acids and most healthy individuals can get sufficient amounts regardless of their type of diet. Carnitine helps in the production of energy in the cell. It is involved in bringing long-chain fatty acids to the mitochondria — “the powerhouse” of the cell — which are then utilized for energy through oxidation. It also keeps potential waste from accumulating in the mitochondria so it performs more efficiently. Thus, it may have antioxidant properties (ods.od.nih.gov/factsheets).

So why is all of this important? L-carnitine may play a role in several chronic diseases, such as heart disease, type 2 diabetes, high blood pressure and even fatty liver disease.

Let’s look at the evidence.

Heart disease

There are two studies with conflicting results on heart disease. In one study, the results are negative, while the other study shows beneficial results. How could that be the case?

In the first study, L-carnitine appears to increase the risk of heart disease through the development of atherosclerosis, or plaque deposits, in the arteries (Nat Med Online. 2013 April 7). L-carnitine is found in foods such as red meat. In this study, mice and healthy human volunteers who regularly ate red meat were observed. Interestingly, the bacteria in the gastrointestinal tract, or gut, in those who consumed red meat were such that L-carnitine was broken down into a metabolite called trimethylamine-N-oxide (TMAO).

This metabolite was then found to increase cholesterol deposits in the arterial walls of mice. In other words, TMAO may promote the development of atherosclerosis. In humans, there was a predicted elevated risk of developing cardiovascular disease and cardiac events, such as heart attacks, strokes and death after three years, but like the mice, only in those that had elevated TMAO levels.

Also of interest, the researchers demonstrated that vegetarians and vegans, when given carnitine supplements, did not produce TMAO. Thus, TMAO production may have to do with microbes that populate the gut of those who consume red meat. This is a preliminary study, mind you, but it makes you wonder if it is the carnitine or the red meat that may be promoting the development of TMAO and the potential for increased atherosclerosis. Carnitine by itself did not cause increased risk of heart disease, but rather the metabolite TMAO did.

In the second study, a meta-analysis (a group of studies) showed those patients given L-carnitine supplements after a heart attack had a statistically significant reduced risk of death from all-causes by 22 percent in 11 trials, ventricular arrhythmias by 65 percent in five trials and chest pain (angina) by 40 percent in two trials (Mayo Clin Proc Online. 2013 April 15).

These were randomized controlled trials (RCTs), the gold standard of studies. The benefits may have been derived from containing the amount of infarct, or dead tissue, in the heart, as well as by increasing the amount of energy in cardiomyocytes (the muscle cells of the heart). In some of the studies, L-carnitine supplements were given for as long as six to 12 months.

Thus, the authors concluded that L-carnitine may be important for those suffering a heart attack, but also in the secondary prevention of a recurrent heart attack. The authors postulated that the mechanism by which L-carnitine derived its beneficial effects was through the improvement in glucose (sugar) utilization in the mitochondria. However, even though it was a meta-analysis, the population size was not large. According to the authors, the patients who might be candidates for carnitine supplementation are those who have had a heart attack and can’t take beta blockers or ACE inhibitors.

Type 2 diabetes

In a meta-analysis (a group of four studies), those given L-carnitine saw an improvement in parameters associated with type 2 diabetes (Exp Clin Endocrinol Diabetes Online. 2013 Feb. 2). There was a significant decrease in fasting glucose (sugar) levels of 14.3 mg/dL and in LDL “bad” cholesterol levels of 8.8 mg/dL. The patients who received L-carnitine were those who were deficient. These studies were RCTs, though they were not large in size.

Role in high blood pressure

In a study involving rats, the results ultimately showed that L-carnitine reduced oxidative stress on the kidneys and helped reverse hypertension-induced kidney damage (Eur J Nutr Online. 2012 Dec. 6). The impact is most likely from the downregulation, or decrease, in inflammatory factors, such as NF-kB, and the upregulation of anti-inflammatory factors, such as NRF2 and PPAR alpha. Thus, L-carnitine may have antioxidant properties that help protect the kidney against damage produced by high blood pressure. These results are exciting, but they are preclinical, or animal-based, and need studies in humans to confirm the results.

Fatty liver disease

As I discussed in last week’s article, fatty liver is a pervasive disease that is benign most of the time, but not always. In a RCT, L-carnitine reduced the liver enzymes significantly (Am J Gastroenterol. 2010;105:1338-1345). These patients had the complication of hepatitis, which was induced by non-alcoholic fatty liver disease. So these were patients on a potentially dangerous road to cirrhosis and, ultimately, to hepatocellular carcinoma (cancer of the liver). In 24 weeks, L-carnitine supplementation not only decreased the liver enzymes, but also cholesterol, glucose and insulin levels. Thus, as the authors concluded, L-carnitine supplementation seemed to improve the overall liver functioning in patients with complications of fatty liver disease.

Though these studies are early or small and more study is warranted, this may be a valuable substance. Thus, it may be worth having your L-carnitine blood levels checked if you have a chronic disease where there might be a deficiency, such as in type 2 diabetes. Check with your physician first, but patients could take L-carnitine supplements if their levels were low or for a protective effect. In cases of heart attacks, high blood pressure and fatty liver disease, carnitine supplementation may decrease organ damage, regardless of your levels.

Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management.   For further information, go to the website www.medicalcompassmd.com and/or consult your personal physician.

When we think of the most prevalent chronic diseases, heart disease, stroke, cancer, diabetes and others come to mind. However, there is also a chronic liver disease — nonalcoholic fatty liver disease — a conglomeration of fats, including triglycerides.

The problem with this disease is that it could lead to nonalcoholic steatohepatitis (fatty liver hepatitis), fibrosis (too much connective tissue due to repair) and eventually cirrhosis, which might ultimately result in cancer (hepatocellular carcinoma).

Fortunately, the risk of going down this dangerous path is relatively small. Most of the time, it remains a mild fatty liver disease.

Although it is rare, a study presentation in 2012 at the American Association for the Study of Liver Diseases suggested that NAFLD was the third most common risk for hepatocellular carcinoma behind infection and alcohol abuse (AASLD. 2012 Nov. 11; Abstract 97). Some study patients with hepatocellular carcinoma progressed to this level without first having cirrhosis. Those patients who developed liver cancer but did not have cirrhosis were more likely to have diabetes, obesity, high blood pressure and/or a high cholesterol profile. NAFLD occurs more frequently in males than females, and it needs to be taken very seriously.

The prevalence of NAFLD, which is benign in most cases, is relatively high, with estimates ranging from 10 to 46 percent (Gastroenterology. 2011; 140:124-131). In fact, a recent study shows that adolescents between the ages of 12 and 18 have seen a threefold increase in NAFLD, from 3.3 percent to almost 10 percent, in the last 20 years, according to data from the National Health and Nutrition Examination Survey (DDW. 2012 May 18; Abstract 705). This correlated primarily with obesity, but the rise outstrips the rate of increase in obesity in this adolescent population.

How is it diagnosed?

When liver enzymes are elevated, usually two to five times normal, then it tends to be more commonly diagnosed (Hepatology. 2003; 37:1286-1292). These liver enzymes include aspartate aminotransferase and alanine aminotransferase. What makes this disease diagnosis more difficult is that patients without elevated liver enzymes may have the disease and, in most cases, they have no symptoms.

The gold standard of diagnosis is through a liver biopsy, though this is invasive and thus has its dangers. Another method is through ultrasound, a first-line diagnosis method. Ultrasound is 60 to 94 percent sensitive and 66 to 95 percent specific (J Hepatol. 2009; 51:433–445). Though it is not the most accurate, it has the fewest side effects. Ultrasound is also technician-dependent in terms of grading the amount of fatty infiltrates in the liver — mild, moderate and severe. Unfortunately, the milder the amount of fatty infiltrates, the less accurate the reading. Other methods for diagnosis include transient elastography, computed tomography and magnetic resonance.

What might be the cause?

What is the potential cause? One theory is that intraperitoneal fat (visceral fat or central obesity) infiltrates the liver through the portal vein, resulting in insulin resistance and fatty liver (Arterioscler Thromb Vasc Biol. 1990; 10:493-496). Therefore, it is not surprising that, along with insulin resistance, there is glucose intolerance. High triglycerides and low HDL (“good”) cholesterol are also commonly associated with the disease (Gastroenterology. 1999; 116:1413–1419).

How can we alter this disease?

The good news is that NAFLD is potentially reversible through lifestyle modifications, including changes in diet and an increase in exercise.

With exercise, the premise is that the more activity a patient gets, the higher the probability of metabolizing the liver fat.

In an epidemiologic study of over 3,000 patients using data from NHANES, results showed that those with NAFLD are significantly less active than those without the disease. It did not matter the type of activity, NAFLD patients did less of it. In fact, patients who had both diabetes and NAFLD were found to do the least amount of physical activity (Aliment Pharmacol Ther. 2012; 36:772-781). The scary aspect is that patients with NAFLD have a significant eight times increased risk of cardiovascular death between the ages of 45 and 54 (Am J Gastroenterol. 2008; 103:2263–2271). And we know activity improves cardiovascular results.

In a meta-analysis (a group of 23 studies ranging from one to six months in duration) that used the Cochrane database, the results showed a significant reduction in fat content in the liver and a decrease in liver enzymes when lifestyle modifications were employed (J Hepatol. 2012 Jan.; 56:255-266). Reduction in weight had the most substantial correlation with the results. Of the 23 studies, five that looked at liver cells on a microscopic level showed a reduction in inflammation that occurred with lifestyle changes. In addition, there were also improved glucose levels and sensitivity to insulin after the modifications.

Benefits of coffee

In yet another study, coffee was shown to reduce the risk of NAFLD developing into fibrosis, a more advanced stage liver disease, by a substantial 36 percent (AASLD. 2012 Nov. 11; Abstract 99). However, weaknesses in this trial were that it was unclear how many cups of coffee were needed to have this effect and whether the coffee needed to include caffeine. The researchers theorize that there are hundreds of compounds in coffee, such as vitamins, minerals, phenolic compounds, lignans and quinides that may have this effect, not just caffeine.

In my practice, I have seen several patients with liver enzymes elevated to at least twice normal levels. After following a nutrient-dense, plant-rich diet, they saw their liver enzymes significantly reduced or returned to normal levels within a few months. One patient’s liver enzymes had been raised for 20 years without a known cause, and a first-line relative had recently been diagnosed with liver cancer.

If you have risk factors for nonalcoholic fatty liver disease, such as obesity, diabetes, high blood pressure and high cholesterol, I recommend having your liver enzymes checked on a regular basis. Those with family histories of elevated liver enzymes and hepatocellular carcinoma (liver cancer) may also want to get a scan, at least with ultrasound.

The best way to treat NAFLD is with lifestyle modifications, and while it is never too late to treat NAFLD, it is better to discover the disease earlier to reduce your risk of complications. If you are obese, NAFLD is one more important reason to transform your body composition by reducing fat mass.

Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management. For further information, go to the website www.medicalcompassmd.com and/or consult your personal physician.